**7. Conclusions**

PASK function could be critical for preserving the nutrient effect on hypothalamic AMPK and mTORC1/S6K1 pathways and maintain the regulatory role of GLP1/exendin-4 in food intake.

PASK regulates the hepatic glucose sensor GCK and AKT, an insulin signaling intermediators, and glucose and lipidic metabolism through the regulation of the key genes and proteins required during hepatic fasting/feeding adaptation. Moreover, PASK deficiency improves mitochondrial biogenesis and antioxidant mechanisms.

HFDs alter the adaptive response of *Pask* gene expression to fasting/feeding. PASK deficiency eliminates many of the harmful effects HFDs have on the liver, thereby decreasing the lipid depots. PASK deficiency decreases the expression of several transcription factors stimulated under fasted conditions to promote the expression of the gluconeogenic enzymes and those promoting the expression of

**359**

**Author details**

and Carmen Sanz1,2

Madrid, Madrid, Spain

Madrid, Madrid, Spain

Verónica Hurtado-Carneiro1,3\*, Ana Pérez-García1

The authors declare no conflict of interest.

University Complutense of Madrid, Madrid, Spain

\*Address all correspondence to: verohur@ucm.es

provided the original work is properly cited.

1 Department of Biochemistry and Molecular Biology, Faculty of Medicine,

2 Department of Cellular Biology, Faculty of Medicine, University Complutense of

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

3 Department of Physiology, Faculty of Medicine, University Complutense of

, Elvira Álvarez1

*Role of Nutrient and Energy Sensors in the Development of Type 2 Diabetes*

We thank Pilar Dongil for their contribution to this work.

lipogenic genes after feeding that are significantly overstimulated in wild type

PASK deficiency avoids insulin resistance and glucose intolerance during aging, preventing an age-related decrease in the expression of several antioxidant enzymes

All these actions make PASK a significant pharmacological target for diseases, such as obesity and diabetes, and for preventing some of the more harmful effects

This work was supported by grants from the Complutense University-Banco Santander Funding Programme for the Creation and Consolidation of Research

*DOI: http://dx.doi.org/10.5772/intechopen.95454*

and improving mitochondrial function.

HFD-fed mice.

of aging.

Teams.

**Acknowledgements**

**Conflict of interest**

*Role of Nutrient and Energy Sensors in the Development of Type 2 Diabetes DOI: http://dx.doi.org/10.5772/intechopen.95454*

lipogenic genes after feeding that are significantly overstimulated in wild type HFD-fed mice.

PASK deficiency avoids insulin resistance and glucose intolerance during aging, preventing an age-related decrease in the expression of several antioxidant enzymes and improving mitochondrial function.

All these actions make PASK a significant pharmacological target for diseases, such as obesity and diabetes, and for preventing some of the more harmful effects of aging.
